Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies
Pedro Piccardo , Larisa Cervenakova, Irina Vasilyeva, Oksana Yakovleva, Igor Bacik, Juraj Cervenak, Carroll McKenzie, Lubica Kurillova, Luisa Gregori, Kitty Pomeroy, and David M. Asher
Author affiliations: University of Edinburgh, Easter Bush, UK, (P. Piccardo); Food and Drug Administration, Kensington, Maryland, USA (P. Piccardo, I. Bacik, J. Cervenak, L. Kurillova, L. Gregori, K. Pomeroy, D.M. Asher); Holland Laboratory American Red Cross, Rockville, Maryland, USA (L. Cervenakova, I. Vasilyeva, O. Yakovleva, C. McKenzie)
Figure 2. Histopathologic analysis of squirrel monkey inoculated with bovine spongiform encephalopathy agent (A, B). Spongiform degeneration in the cerebral cortex (A), adjacent section showing abundant prion protein (PrP) immunopositivity (B). Squirrel monkey without transmissible spongiform encephalopathy (C, D). Cerebral cortex with no spongiform degeneration (C), absence of PrP positivity in the cerebral cortex (D). Panels A and C correspond to sections stained with hematoxylin and eosin; panels B and D were sections immunostained with PrP antibody 6D11. Scale bars = 150 μm.
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